2.2 Nutrient Functions, Deficiencies & Toxicities
Key Takeaways
- Fat-soluble vitamins (A, D, E, K) are stored in the body and carry the greatest toxicity risk, while water-soluble vitamins (B-complex and C) are generally excreted and require regular intake.
- Classic deficiency syndromes are high-yield: scurvy (vitamin C), beriberi (thiamin/B1), pellagra (niacin/B3 — the 3 Ds: dermatitis, diarrhea, dementia), and rickets/osteomalacia (vitamin D).
- Iron-deficiency anemia is microcytic and hypochromic, whereas vitamin B12 and folate deficiencies cause macrocytic (megaloblastic) anemia — only B12 deficiency adds neurologic damage.
- Sodium, potassium, calcium, and magnesium are the major electrolytes whose lab values drive nutrition diagnoses in clinical practice.
- Vitamin and mineral toxicities matter on the RD exam: vitamin A is teratogenic in excess, excess vitamin D causes hypercalcemia, and high iron is acutely toxic, especially in children.
Micronutrients show up across both Domain 1 and the clinical scenarios in Domain 2. The exam rewards pattern recognition: match a deficiency sign to its nutrient, name the function, and know the food sources. Start by splitting vitamins into fat-soluble (A, D, E, K) and water-soluble (B-complex and C).
Fat-soluble vitamins are absorbed with dietary fat (and depend on bile and a functioning ileum), stored in the liver and adipose tissue, and therefore carry a real toxicity risk. Water-soluble vitamins are not stored in large amounts and excess is excreted in urine, so deficiency develops faster but toxicity is rarer. A practical corollary: patients with fat malabsorption (cystic fibrosis, Crohn's disease, cholestasis, pancreatic insufficiency, or after bariatric surgery) are at high risk for A, D, E, and K deficiency, and any of these conditions in a stem should prompt you to think fat-soluble vitamins first.
Fat-Soluble Vitamins (A and D)
| Vitamin | Function | Deficiency | Toxicity | Sources |
|---|---|---|---|---|
| A (retinol) | Vision, epithelial integrity, immunity | Night blindness, xerophthalmia, Bitot's spots | Teratogenic (avoid high-dose in pregnancy); liver/bone damage, intracranial pressure | Liver, dairy, eggs; beta-carotene from orange/dark-green produce |
| D (calciferol) | Calcium/phosphorus absorption, bone mineralization | Rickets (children), osteomalacia (adults), hypocalcemic tetany | Hypercalcemia, soft-tissue calcification, kidney stones | Fortified milk, fatty fish, egg yolk, UVB sunlight |
Two high-yield traps: pre-formed vitamin A (retinol from liver and supplements) is the teratogenic form, whereas beta-carotene from plants is converted only as needed and is not teratogenic. And vitamin D is functionally a hormone — calcitriol (1,25-dihydroxyvitamin D) raises serum calcium by increasing intestinal absorption, so vitamin D toxicity presents as hypercalcemia, not low calcium.
Fat-Soluble Vitamins (E and K)
| Vitamin | Function | Deficiency | Toxicity | Sources |
|---|---|---|---|---|
| E (tocopherol) | Antioxidant; protects polyunsaturated membrane lipids | Hemolytic anemia (premature infants), peripheral neuropathy (rare) | May impair platelet aggregation / clotting at very high doses | Vegetable oils, nuts, seeds, wheat germ |
| K (phylloquinone, menaquinone) | Synthesis of clotting factors II, VII, IX, X | Easy bruising, prolonged prothrombin time, bleeding; hemorrhagic disease of the newborn | Low toxicity risk | Leafy greens (kale, spinach); synthesized by gut bacteria |
The clinically critical interaction: vitamin K antagonizes warfarin. Patients on warfarin should keep vitamin K intake consistent rather than eliminating greens — large swings in leafy-green intake destabilize the INR. A sudden increase in vitamin K lowers the INR (more clotting); a sudden decrease raises it (more bleeding). Newborns receive a prophylactic vitamin K injection because their guts are not yet colonized by K-producing bacteria.
Water-Soluble Vitamins: B-Complex (Energy and Blood)
| Vitamin | Key Function | Deficiency Syndrome | Food Sources |
|---|---|---|---|
| B1 Thiamin | Carbohydrate metabolism, nerve function | Beriberi (wet = cardiac, dry = neuropathic); Wernicke-Korsakoff in alcoholism | Pork, enriched grains, legumes, sunflower seeds |
| B2 Riboflavin | Energy metabolism via FAD/FMN | Cheilosis, angular stomatitis, glossitis, photophobia | Milk, eggs, organ meats, enriched grains |
| B3 Niacin | Energy metabolism via NAD/NADP | Pellagra — the 3 Ds: dermatitis, diarrhea, dementia (and death) | Meat, fish, peanuts; synthesized from tryptophan |
| B6 Pyridoxine | Amino acid metabolism, heme/hemoglobin synthesis | Microcytic anemia, dermatitis, peripheral neuropathy, convulsions | Poultry, fish, potatoes, bananas, chickpeas |
Note that isoniazid (INH) for tuberculosis depletes B6, so supplementation is standard — a tested medication-nutrient interaction. Thiamin is given before glucose in suspected alcohol-use disorder to prevent precipitating acute Wernicke encephalopathy.
Folate, B12, and Vitamin C
| Vitamin | Key Function | Deficiency Syndrome | Food Sources |
|---|---|---|---|
| B9 Folate | DNA synthesis, red cell formation | Megaloblastic anemia; neural tube defects (spina bifida) if low periconceptionally | Leafy greens, legumes, liver, fortified grains |
| B12 Cobalamin | Nerve myelin, DNA synthesis (with folate) | Megaloblastic anemia plus neurologic damage; pernicious anemia when intrinsic factor is lacking | Animal foods only — meat, fish, eggs, dairy |
| C Ascorbic acid | Collagen synthesis, antioxidant, enhances non-heme iron absorption | Scurvy: bleeding gums, poor wound healing, corkscrew hairs, perifollicular hemorrhage | Citrus, berries, peppers, broccoli, potatoes |
Folic acid fortification of enriched grains is mandated in the U.S. precisely to prevent neural tube defects, and women capable of pregnancy are advised to get 400 mcg/day. Because B12 is found only in animal foods, strict vegans need fortified foods or supplements. Pairing vitamin C with a plant iron source (e.g., orange juice with fortified cereal) sharply boosts non-heme iron uptake — a counseling point and a frequent question.
Major Minerals (Electrolytes and Bone)
Major minerals are needed in larger amounts (>100 mg/day) and dominate clinical electrolyte management.
| Mineral | Function | Deficiency / Clinical Note | Sources |
|---|---|---|---|
| Calcium | Bone/teeth, muscle contraction, clotting, nerve signaling | Osteoporosis; tetany if serum ionized calcium drops | Dairy, fortified plant milks, tofu, leafy greens |
| Sodium | Fluid balance, nerve impulse, acid-base | Hyponatremia (confusion, seizures); chronic excess raises blood pressure | Table salt, processed and cured foods |
| Potassium | Fluid balance, cardiac rhythm, muscle | Hypo- and hyperkalemia both cause arrhythmias; DASH diet emphasizes K+ | Bananas, potatoes, oranges, beans, tomatoes |
| Magnesium | Cofactor for 300+ enzymes, ATP, nerve/muscle | Weakness, arrhythmia, tetany, refractory hypokalemia/hypocalcemia | Nuts, whole grains, legumes, dark greens |
The Dietary Guidelines set sodium at less than 2,300 mg/day for adults. Watch for refeeding syndrome, where rapidly fed malnourished patients develop dangerous drops in phosphorus, potassium, and magnesium as insulin drives these ions intracellularly.
Trace Minerals
Trace minerals are needed in milligram or microgram amounts but have outsized clinical effects.
| Mineral | Function | Deficiency / Note | Sources |
|---|---|---|---|
| Iron | Hemoglobin and myoglobin oxygen transport | Microcytic, hypochromic anemia; supplements are a leading cause of acute pediatric poisoning | Heme: red meat, poultry; non-heme: legumes, fortified grains |
| Zinc | Immunity, wound healing, growth, taste | Poor healing, hypogeusia (loss of taste), growth retardation, dermatitis | Oysters/shellfish, red meat, legumes, seeds |
| Iodine | Thyroid hormone (T3, T4) synthesis | Goiter in adults; cretinism (irreversible) in infants | Iodized salt, seafood, dairy, seaweed |
Heme iron (from animal flesh) is far better absorbed than non-heme iron (from plants); absorption of non-heme iron is enhanced by vitamin C and inhibited by phytates, tannins (tea/coffee), and calcium taken together. Selenium and copper round out the high-yield trace minerals — copper deficiency can itself cause anemia and neutropenia, and excess zinc supplementation can induce copper deficiency.
Diagnosing by Anemia Type
A frequently tested distinction is the type of anemia a deficiency produces, classified by red-cell size (mean corpuscular volume, MCV):
- Microcytic, hypochromic (small, pale cells; low MCV) → iron deficiency (most common worldwide); also vitamin B6 deficiency and lead poisoning. Check ferritin (low) and total iron-binding capacity (high).
- Macrocytic / megaloblastic (large cells; high MCV) → folate (B9) or vitamin B12 deficiency, both of which impair DNA synthesis in developing red cells.
- Normocytic → acute blood loss or anemia of chronic disease.
The classic trap: only B12 deficiency adds neurologic signs (numbness, paresthesias, gait disturbance, dementia) because B12 maintains myelin. Giving folate alone to a B12-deficient patient can correct the megaloblastic anemia on a blood smear yet allow the underlying neurologic damage to progress silently — which is why you must check B12 status, not just treat the anemia. Always tie the lab finding to the nutrient mechanism rather than memorizing values in isolation.
A patient presents with bleeding gums, poor wound healing, and corkscrew hairs. Which nutrient deficiency is most consistent with this presentation?
Which vitamin deficiency causes a macrocytic (megaloblastic) anemia accompanied by neurologic symptoms such as numbness and impaired gait?